Quantifying Macrophage Presence of Retinal Tissue Sections in a Stargardt Disease Mouse Model

dc.contributor.authorGeczi, Caitlin
dc.date.accessioned2025-05-07T16:25:49Z
dc.date.available2025-05-07T16:25:49Z
dc.date.issued2025
dc.description.abstractThis project aims to quantify macrophage presence in a Stargardt disease (STGD1) mouse model after inducing photooxidative damage using a light stress (LS) model. STGD1 is a genetic eye disease that leads to central vision loss due to a loss-of-function mutation of the ABCA4 gene involved in our visual cycle transferring N-retinylidene-phosphtidylethanolamine (N-ret-PE) from the retinal pigmental epithelium (RPE) to the outer segment discs of rods. The accumulation of N-ret-PE and RPE damage due to photooxidative stress triggers the complement system cascade of our innate immune system. Activation of the complement system leads to an immune response led by macrophage recruitment so they can engulf foreign pathogens and debris from cell death. Retinal tissue sections were prepared following LS and underwent immunohistochemistry using macrophage-specific marker, Iba1. The entire eyecup was then imaged using fluorescent confocal microscopy (Nikon C2). Next, I’m working to quantify Iba1 labeling in the retinal and subretinal layers to perform two sets of parameters: loose settings (to capture all Iba1 labeling) and stringent settings (aiming to increase specificity for whole macrophages). This research will give us a better understanding of the role of macrophages in response to photooxidative damage for mechanisms of STGD1 to generate potential therapy options to treat STGD1.
dc.description.reviewstatusReviewed
dc.description.scholarlevelUndergraduate
dc.description.sponsorshipJamie Cassels Undergraduate Research Awards (JCURA)
dc.identifier.urihttps://hdl.handle.net/1828/22174
dc.publisherUniversity Of Victoria
dc.subjectStargardt disease
dc.subjectcomplement system
dc.subjectphotooxidative stress
dc.subjectmacrophage
dc.subjectIba1
dc.titleQuantifying Macrophage Presence of Retinal Tissue Sections in a Stargardt Disease Mouse Model
dc.typePoster

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